1. Field of the Invention
The present invention relates to a method and apparatus for maximizing stroke volume through atrioventricular pacing using an implanted cardioverter/pacer.
2. Description of the Prior Art
The ability to control heart rate by means of electrical stimulation has given the cardiologist an important tool for the management of patients suffering from abnormal heart functioning. Medical technology has developed to the point that battery-operated pacers, both temporary and implantable, are available with characteristics suitable for various clinical situations. The operation of such heart pacers (also known as pacemakers) presupposes basic understanding of the functioning of the heart.
The heart is divided into a left atrium, right atrium, left ventricle and right ventricle, and contains a sinoatrial (SA) node, which is a region of specialized tissue in the wall of the right atrium. This is the natural pacemaker of the heart, in that it emits a series of electrical pulses, each of which triggers a cycle of cardiac activity. As the pulse from the SA node spreads across the atrial walls, it initiates atrial contraction to pump blood into the ventricles. The pulse is then detected by another area of specialized tissue, known as the atrioventricular (AV) node, and is then conducted through special pathways of conductive tissue to the ventricles. While the pulse passes through the conductive tissues to the walls of the ventricles, atrial contraction moves blood into the ventricles. By the time ventricular contraction begins (as a result of arrival of the pulse at the ventricles), the ventricles are expanded and ready to pump blood into the lungs and the circulatory system of the body. After each contraction, the heart relaxes, the atria refill with blood, and another pulse is generated in the SA node so as to start the next cycle of cardiac activity.
Normal rhythm (known as "sinus rhythm") originates in the SA node of the heart. However, disorders of rhythm (known as "arrhythmias") may occur. For example. if the conductive pathways to or in the ventricles are for any reason disrupted, atrial-generated pulses may no longer trigger ventricular activity, and ventricular contraction may no longer be synchronized with atril activity. There are numerous arrhythmias wherein the normally sequential contractions of the atria and the ventricles are absent. Such arrhythmias have led to the development of the electronic pacemaker, which takes over the task of stimulating the ventricles to contract at a normal rate (for example, 70 beats per minute). In the modern demand electronic pacemakers, operation is typically synchronized with the heart's electrical activity through electrocardiograph (ECG) monitoring.
The normal ECG consists of a series of voltage changes resulting from the contraction of the atria and the contraction and recovery of the ventricles in the heart. A normal electrocardiogram derived from ECG monitoring includes a series of spaced waveform regions known as the QRS complex, consisting of: a small upward deflection (the P wave), due to atrial contraction; a brief downward swing (the Q wave), followed by a large upward swing (the R wave), and then a further downward swing (the S wave), resulting from ventricular contraction; and a small upward deflection (the T wave), indicating recovery of the ventricles. Thus, disturbances of the conducting mechanism or pathways between the atria and the ventricles (known as "heart blocks") can be detected by ECG monitoring. When the rate of conduction from the AV node down through the conductive pathways is prolonged, the P-R interval is longer than normal, and this is called a first degree atrioventricular (AV) block. Another type of arrhythmia (incomplete heart block or second degree block) occurs when the ventricles do not respond to every atrial beat. Such a situation can be caused by too fast an atrial rate, or by a diseased AV pathway, and can be detected by ECG monitoring. Finally, a complete heart block (or complete AV dissociation) occurs when the main conducting pathway between the atria and ventricles is interrupted. In such situation, the atria continue to beat normally, but the ventricles beat at their own, often very slow, escape rate, and such a situation can also be detected by ECG monitoring. Occurrence of any of the latter conditions indicates need for artificial stimulation of the heart.
The concept of atrioventricular (AV) pacing was developed to combat the latter-noted heart disturbances. As an example, one type of AV pacer typically operates as follows. The AV pacer monitors the electrical activity of the heart and awaits a ventricular contraction (as indicated by an R wave in the ECG). If no ventricular contraction occurs after a first period of time (known as the "atrial escape interval"), the pacer issues a stimulation pulse, which is applied to the atrium of the heart. Then, the pacer again awaits a ventricular contraction. If, by the end of a second period of time (known as the "ventricular escape interval") there is no ventricular contraction, a ventricular stimulation pulse is generated, and is applied to the ventricle of the heart. The difference in time between the atrial escape interval and the ventricular escape interval equals the delay between issuance of the atrial pulse and the ventricular pulse, and is known as the "AV delay." The normal heart typically issues atrial and ventricular pulses with a natural AV delay of 150-250 milliseconds.
In the modern AV pacer, the electronics are preprogrammed so that a fixed AV delay is set into the device, typically in the range of the aforementioned 150-250 milliseconds. Because hearts vary from individual to individual, a given AV delay may be optimum for one person, while the same delay may be only adequate for another. This less than optimum timing of the ventricular stimulation pulse could result in less than optimum pumping action by the paced heart. There is a need, therefore, for an electronic pacer which maximizes the amount of blood pumped by the heart (or "stroke volume") for each ventricular stimulation pulse.